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pubmed:abstractText |
Activation of T-cells infected by HIV-1 results in activation of long terminal repeat (LTR)-dependent viral transcription and ultimately the production of infectious virus. Although full T-cell activation requires a complex series of intracellular signals, including protein kinase C activation, calcium mobilisation, and less-well defined lymphokine-induced signals, the HIV-1 LTR can be activated by subsets of these signals. We have studied the interaction of these signals in the human lymphoma line, Jurkat, in activation of the HIV-1 LTR. The HIV promoter was induced by IL-1 and phorbol ester activation of PKC but not by a calcium ionophore. The constitutively active form of Ha-ras could replace phorbol ester stimulation of the HIV promoter and of a synthetic promoter containing NF kappa B binding sites.
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